{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T19:00:31Z","timestamp":1785438031554,"version":"3.56.0"},"reference-count":33,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2025,9,9]],"date-time":"2025-09-09T00:00:00Z","timestamp":1757376000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,9,9]],"date-time":"2025-09-09T00:00:00Z","timestamp":1757376000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2025,9,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      Invasive pulmonary aspergillosis (IPA) is a severe fungal disease caused by\n                      <jats:italic toggle=\"yes\">Aspergillus fumigatus<\/jats:italic>\n                      (\n                      <jats:italic toggle=\"yes\">Af<\/jats:italic>\n                      ) that may spread hematogenously to extrapulmonary organs. IPA is typically associated with a broad spectrum of immunocompromised conditions and constitutes a high mortality rate. While the association of influenza as a risk for secondary bacterial infections is well appreciated, emerging evidence indicates that influenza-hospitalized patients demonstrate increased susceptibility to severe aspergillosis infection. In this study, we developed a murine Influenza A Virus (IAV)-\n                      <jats:italic toggle=\"yes\">Af<\/jats:italic>\n                      co-infection model and investigated the role of IAV host response in promoting invasive\n                      <jats:italic toggle=\"yes\">Af<\/jats:italic>\n                      infection. Our data show that IAV temporarily suppresses neutrophil recruitment in the early phase of\n                      <jats:italic toggle=\"yes\">Af<\/jats:italic>\n                      co-infection (24 hours), followed by a subsequent increase in neutrophil levels (48 hours). RNA sequencing analysis of neutrophils from IAV-\n                      <jats:italic toggle=\"yes\">Af<\/jats:italic>\n                      co-infected lungs (48 hours) reveals enrichment of pathways regulating inflammatory responses and phagocytosis. Despite higher inflammatory response and phagocytosis, the host response from IAV-\n                      <jats:italic toggle=\"yes\">Af<\/jats:italic>\n                      co-infected lungs had suppressive effects on neutrophil conidial killing, correlating with lung fungal load and invasion. However, the increased fungal invasion observed at 24 hours post co-infection, despite similar fungal loads in both groups (\n                      <jats:italic toggle=\"yes\">Af<\/jats:italic>\n                      vs. IAV-\n                      <jats:italic toggle=\"yes\">Af<\/jats:italic>\n                      ), suggests that IAV-induced pathologic lung inflammation and vascular damage likely promote\n                      <jats:italic toggle=\"yes\">Af<\/jats:italic>\n                      invasiveness during the initial phase of co-infection, and subsequently, the defects in neutrophil fungicidal response and exacerbated lung damage lead to sustained and fatal IPA pathogenesis in the later phase of co-infection.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/iai.00234-25","type":"journal-article","created":{"date-parts":[[2025,8,11]],"date-time":"2025-08-11T13:36:06Z","timestamp":1754919366000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":4,"title":["Loss of pulmonary tissue protection and neutrophil microbicidal defects promote severe\n                    <i>Aspergillus fumigatus<\/i>\n                    infection during influenza A virus infection"],"prefix":"10.1128","volume":"93","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3617-477X","authenticated-orcid":false,"given":"Zhihan","family":"Wang","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/04a5szx83","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota","place":["Grand Forks, 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